1. Field of the Invention
This invention relates generally to percutaneous transluminal catheters used for the clinical treatment of a coronary and vascular deficiency, and particularly to a catheter for the antegrade perfusion of an ischemic region of the myocardium induced by a coronary or vascular deficiency.
2. Prior Art
The treatment of coronary or vascular defects and diseases represents a significant portion of the current expenditure in critical care time and resources, however both the short- and long-term success or survival rates among afflicted patients remains surprisingly far below the expectations of most practitioners.
Accepted treatments encompass a wide spectrum of modalities depending upon the type and severity of the coronary deficiency, from heart transplants, bypass surgery, intra-aortic balloon pumping, angioplasty, atherectomy, and thrombolytic drug treatment. These procedures each have incumbent risks and limitations, and their use is frequently dictated by the circumstances of the patient's immediate acute condition, and the available time, equipment, and personnel that can be utilized. Somewhat unexpectedly, the current research and literature suggest that relative success rates for less invasive or complicated procedures may not be significantly different than expensive and complex options such as bypass surgery.
One option that is the subject of current research is perfusing blood from a femoral artery through the distal tip of an angioplasty catheter during the angioplasty procedure. The goal is to minimize the deleterious effects of further blocking a stenosed arterial vessel with the inflated angiolasty balloon, usually for the 3 to 10 minute inflation period required to perform the compressive angioplasty procedure.
Another option is perfusing blood to a proximal site within the aorta or myocardium at an elevated pressure to induce increased circulation in the secondary or tertiary collaterals directly surrounding the ischemic region. This procedure relies on the presence and degree of the patient's existing collateral circulation within substantially the same collateral bed as the "culprit" or afflicted arterial vessel.
The present invention is directed to the principle that the most dramatic and life-threatening effects of a coronary or vascular deficiency may be minimized significantly by providing oxygenated blood to ischemic regions of the myocardium (or other organs or muscle tissue) induced by the deficiency. Such deficiencies can include an athesclerotic lesion or stenosis, thrombus, embolism, vessel spasm, or other types of a restriction in or obstruction of an arterial vessel.
One representative example is the pathogenesis of cardiogenic shock complicating myocardial infarction, wherein the obstruction of a major coronary artery leads to myocardial ischemia--thereby triggering a downward spiral of reduced contractile mass leading to decreased left ventricular function and a corresponding decline in arterial pressure and reduced coronary perfusion, prompting a further reduction in contractile mass, decreasing left ventricular function, declining arterial pressure, and diminishing coronary perfusion--eventually leading to the death of the patient unless the spiral is interrupted and reversed by homeostatic mechanisms or an external therapeutic force.
Cardiogenic shock may also cause the death of a patient who initially survives a moderate or less severe episode of arterial obstruction but then progresses to experience a recurrent arterial obstruction or plural obstructions. This may occur despite aggressive intervention such as coronary angioplasty or bypass surgery. The degree to which cardiogenic shock affects the viability of any eventual therapy depends on the rate of the downward spiral, the length of time which elapses, and the effectiveness of the measures employed to reverse the cardiogenic shock prior to or during the restoration of normal circulation. Even if the therapy proves successful in the short-term, the chances for long-term survival can be significantly diminished (and permanency of any deleterious effects of the infarction significantly magnified) by the progress of cardiogenic shock during the lapse in time between the initial onset of the arterial deficiency and the eventual application of a comprehensive treatment modality.
It has been shown in the literature that survival following myocardial infarction is directly related to the degree of remaining viable myocardium. For example, patients surviving myocardial infarction with severely decreased heart function have greater than 70% mortality by 5 years. By comparison, patients who survive myocardial infarction with minimal damage to the heart may have an 80-90% chance of 5 year survival. Consequently, even intermediate success in lowering the extent of infarction damage can have a dramatic impact on patient survival rates, the extent of interventional and long-term care required for a patient, and the quality of life experienced by that patient.